# Investigating the genetic basis of susceptibility to amoebic gill disease and idiopathic gill lesions in Atlantic salmon populations using field data

## TL;DR

This study identifies genetic regions linked to gill disease susceptibility in Atlantic salmon, offering insights for improving disease resistance in aquaculture.

## Contribution

The study reports novel QTL regions and candidate genes associated with susceptibility to amoebic gill disease and idiopathic gill lesions in Atlantic salmon.

## Key findings

- A QTL on chromosome 12 is associated with susceptibility to amoebic gill disease (AGD).
- Two QTL regions on chromosomes 2 and 12 are linked to idiopathic gill lesions (IGL).
- Candidate genes like tfeb, zscan12l, and ifi44l are implicated in immune-related functions.

## Abstract

Gill-related morbidity and mortality have become a major concern to the Atlantic salmon industry worldwide. Understanding the genetic mechanisms underlying susceptibility to gill diseases or lesions can help guide mitigation efforts. Genome-wide association analysis was conducted on gill scores from two large cohorts of Atlantic salmon populations, reared in Norway and Canada, that were phenotyped during amoebic gill disease (AGD) outbreaks and at harvest (referred to as idiopathic gill lesions (IGL)), respectively.

Whereas one novel quantitative trait locus (QTL) region on chromosome 12 was associated with susceptibility to AGD, two QTL regions on chromosomes 2 and 12 were associated with IGL. There was an overlap between the QTL region on chromosome 12 for AGD and IGL. The lead variant(s) identified explained approximately 7% of the additive genetic variance for AGD, and 3 and 10% for IGL, for the QTL on chromosomes 2 and 12, respectively. Putative candidate genes identified within or close to the lead variants include tfeb, zscan12l, and ifi44l, with the majority of these genes playing roles relating to immune functions. Fine-mapping the identified QTL region associated with AGD using re-sequence data revealed a lead intergenic variant explaining 9% of the additive genetic variance.

Our results provide valuable insight into the genetic architecture of susceptibility to AGD and IGL, suggesting that both traits may be partly under the same genetic control. Future studies are warranted, especially on the genetic correlation between AGD and IGL.

The online version contains supplementary material available at 10.1186/s12711-025-01025-6.